Risk factors related to aggressive condylar resorption after orthognathic surgery for females: retrospective study.

OBJECTIVE: The aim of the present study was to identify the risk factors for aggressive condylar resorption (ACR) after orthognathic surgery. METHODS: A total of 25 female patients with osteoarthritis (OA) scheduled for orthognathic surgery were divided into two groups: those who exhibited ACR (ACR (+), n = 8) and those who did not exhibit ACR (ACR (-), n = 17) after surgery. Clinical indices were used to determine the extent of mandibular advancement, the presence of temporomandibular disorder (TMD), and relevant medical treatment histories (including the use of oral contraceptive (OC) medication. TMJ dysfunction was clinically evaluated in terms of pain, the presence of sounds (clicks or crepitus), and disc displacement, joint effusion (JE), and synovial hyperplasia (SH); these were further investigated with the aid of magnetic resonance imaging (MRI). The cephalographic findings were compared with the normal profiles of Japanese subjects. RESULTS: The mean (with SD) extent of mandibular advancement was 11.4 mm (2.4) in ACR (+) and 4.1 mm (1.8) in ACR (-). The TMD medical history of ACR (+) was much more extensive than that of ACR (-); all patients in ACR (+) had a history of OC use. More patients in ACR (+) than in ACR (-) had TMJ dysfunction and disc displacement, JE, and SH on MRI. Preoperative cephalograms showed that ACR (+) patients exhibited counterclockwise rotation of the mandible and retrognathism that was attributable to a small sella-nasion-B (SNB) angle, a wide mandibular plane angle, and a negative inclination of the ramus. CONCLUSIONS: The present findings suggest that the development of ACR after orthognathic surgery to treat mandibular retrognathism may be associated with coexisting TMJ pathologic abnormality.

PR3-ANCA in Wegener's granulomatosis prime human mononuclear cells for enhanced activation via TLRs and NOD1/2.

BACKGROUND: Anti-neutrophil cytoplasmic antibodies (ANCA) is autoantibodies characteristic of vasculitis diseases. A connection between ANCA and Wegener's granulomatosis was well established. The interaction of both ANCA phenotypes (PR3-ANCA and MPO-ANCA) with leukocytes provoked cell activation, which might be involved in the pathogenesis of ANCA-related Wegener's granulomatosis. METHODS: In this study, we examined whether PR3-ANCA sera and purified immunoglobulins from patients with Wegener's granulomatosis prime human monocytic cells for enhanced responses to microbial components in terms of production of proinflammatory cytokines. RESULTS: Flow cytometry demonstrated that stimulation with antibodies to proteinase 3 enhanced the expression of TLR2, 3, 4, 7, and 9, NOD1, and NOD2 in human mononuclear cells. The sera and purified immunoglobulins significantly primed human mononuclear cells to secrete interleukin-8 in response to microbial components via TLRs and NODs. Priming effects were also observed for the production of interleukin-6, monocyte chemoattractant protein-1, and tumor necrosis factor-alpha. On the other hand, PR3-ANCA-negative sera from patients with polyarteritis nodosa which possibly related to MPO-ANCA and aortitis syndrome as well as control sera from a healthy volunteer did not have any priming effects on PBMCs. CONCLUSION: In conclusion, PR3-ANCA prime human mononuclear cells to produce cytokines upon stimulation with various microbial components by up-regulating the TLR and NOD signaling pathway, and these mechanisms may partially participate in the inflammatory process in Wegener's granulomatosis.